Alzheimer's disease (AD) results in progressive loss of cognitive function. The most prevalent model of AD posits that amyloid peptide (AB) accumulates at synapses and prevents synaptic function required for information processing, storage and recovery. The histological hallmarks of AD are amyloid plaque, created by deposition of AB, and tangles created by deposition of hyper phosphorylated tau protein. Therapeutic approaches for AD focus on reduction of AB generation or deposition by inhibition of enzymes that generate AB or by approaches that increase the clearance of AB. Other strategies focus on molecular pathways involved in inflammation. Recent advances in brain imaging using PIB or related tracers allow for an assessment of amyloid load in brain of patients. The diagnosis of AD is also supported by measures of AB40/42 and phosphor tau in the cerebrospinal fluid, however, the magnitude of changes in these markers is modest, and not highly diagnostic in individual patients. With the advent of new therapies for AD there is a major need for simple markers that can be related to the disease pathogenesis and that are sufficiently robust to be useful for diagnosis and monitoring of treatment success.